A Dynamic Syndrome that Ultimately Result in tissue

damage as substrates required for aerobic methabolism

are delivered at an insufficient rate by too little blood
flow or maldistributed flow at the microcelluler level.

1
Hypovolemic Shock

Cardiogenic Shock

Distributive Shock

Obstructive Shock 2
 Hypovolemic Shock

Hemorrhagic shock (most common cause of shock)

Traumatic shock
Nonhemorrhagic shock
Gastrointestinal losses of fluid
Renal losses of fluid
Other

3
 Cardiogenic Shock
Failure of the heart as a pump
Ventricular-outflow impedance
Ventricular-filling impaired
Valvular dysfunction as cause
Failure to generate forward stroke volume

4
 Mixed Shock
Distributive shock states
Septic Shock
Assorted other
Neurogenic Hypothyroidism
Drug overdose Endocrine failure
Anaphylaxis Cyanide poisoning
ARF Ganglionic blockade
HNKC High spinal anesthesia
Liver failure Severe acidosis or alkalosis

5
 Organ Clinical Sign
System Causes
/ Symptom
CNS Changes In Mentation Decreased CPP

CVS Tachycardia Adrenergic Stimulations

Dyshrhytmias Coronary Ischemia
Hypotension Contractility (Ischemia of
MDF/RVF; SVR/preload
Murmur Valvular Dysfunction
or Jugular venous volume/preload / RV failure
pulse
Respiratory Tachypnea Pulmonary Edema
Resp. muscle failure
Sepsis, Acidosis, Hypoxemia 6
 Organ Clinical Sign
System Causes
/ Symptom
RENAL Oligouria Decreased perfuson, afferent
arteriolar constriction

SKIN Cool, clammy, cyanosis, Vasoconstriction, sympathetic

sweating stimulation
OTHER Lactic Acidosis Anaerobic metabolism
Fever Hepatic dysfunction infection

7
Effect Shock to Heart
Hypovolemic Shock

Coronary Perfussion Pressure

Hypotension/Shock P(DAB LV EDV)

Reflex
diastolic filling of
tachycardia/
coronary arteries
bradicardia
CO
Systolic pressure MAP
SVR
8
Effect Shock to Heart
Septic Shock

CO, SVR

Pulmonary Respiratory Failure &

LV EDV P
Edema Concomitant Hypoxemia

DAB P Coronary Hypoperfusion & Myocardial Ischemia

9
Effect Shock to Heart
Cardiogenic Shock
CHF
Dyspnea
Tachypnea
Pulmonary Edema
PaO2
S3 gallop

10
Effect Shock to Renal
Hypotension RBF GFR (< 25-30 ml/hr/70 kg)

Redistribution Cortex To Medulla

Concentrated Urine
(Na < 10mEq/L)

Oligouria
11
By Etiology
Clinical Pathophy-
Shock Type Lab Treatment
Presentation siology
Hypovolemic/ Pallor, fainting, skin Hct, Hgb Blood volume Fluids, Blood,
hemorrhagic clammy, cold; Control blood
tachycardia, loss
hypotension &
Oligouria
Cardiogenic Pallor, fainting, skin CXR, ECG, CO Antidysrhytmics,
clammy, cold; Cardiac vasopressors,
dysrhytmias, enzymes vasodilators,
oligouria, hypotension Ballon support

Septic Fever, chills, warm C&S systemic Antibiotics

skin, tachycardia, Fluids
vascular
oligouria, altered Drain abscesses
mental status, rigor resistance
12
General Criteria
a.Systolic arterial blood pressure is
less then 80 mmHg
b.Oligouria decreased blood level
c. Metabolic acidosis
d.Poor tissue perfussion

13
Baroreceptor Sympathetic N Activity

Cardiac Stimulation Peripheral Vasoconstriction

Cortisol
ACTH & ADH Na + Water Retention RAA Activated

Adrenocortical Epinefrin & Norepinefrin

Vasoactive Hormone Vascular Permeability

Prostaglandisns, histamine, bradykinin,
serotonin, -endorfin, MDF, cachectin 14
Maldistribution of Blood Flow Inadequate O2 Transport

Aerobic met, anaerobic met

Lactic Acid (> 2.5 mmol/L)

ATP Production

Destabilization Mitochondria & RES Rupture of Lysosimes

Endothelial cell Swell
membranes Enzymes
Intracellular Digestion

Phospholipase A2
Activated 15
 ACTH

Adrenocortical Activity 10% Cortisol

blood vol ADH / Vasopressin
Epinefrin & Norepinefrin ( 5 pg/ml)

-Adrenergic Activity

Hydrolysis of phosphatidylinositol
Macula Densa
Ca Intracellular
RAA
Smooth Muscle Contraction
Aldosteron
Smooth Muscle Contraction

Vasoconstriction CO Salt & Water Retention

16
SVR
Blood Losses of about 3 ml/kg Renin

Angiotensin I
More Rapidly in Fast Hemorrhage
Not for symphatic nerve activity Angiotensin II
Vasoconstriction

State of Cold Shock

17
 Epinephrine

> 125 150 pg/ml 1800 pg/ml

400 pg/ml
(4x basal conc) (10x basal conc)

Hyperglycemic Inhibition Insulin Change in Hemodynmic

Lypolytic Release
Ketogenic
Glycolytic SHOCK
Gluconeogenesis
Lactate, Pyruvate, & Alanine

Blood Glucose (Hyperglycemia)

18
Divided into 4 groups :

I. Loss of 10-15% of EBV

II. Loss of 15-25% of EBV (1000 1250 ml loss/kg)

III. Loss of 25-35% of EBV (1250 1750 ml loss/kg)

IV.Loss of 35-45% of EBV (1750 2250 ml loss/kg)

19
Loss of 15-25% of EBV
Moderate shock
Tachycardia
systolic pressure
pulse blood pressure
DABP
Sluggish capillary refill with blanching
Tabletilt Test (+)
Urine Output close to N

20
Loss of 25-35% of EBV
Severe Shock
Skin is cold, clammy and pallid
Blood pressure (30 40%)
DABP 15 20%
Vasoconstriction prominent
Oligouria
CNS confusion to stupor
Tacypnea metabolic acidosis
Pulse rate 120 x/minute

21
Loss of 35-45% of EBV

Profound Shock
Preterminal event
No palpable blood pressure
Loss of peripheral pulse
Loss of carotid arterial pulsations

22
Relationship Between Degree of Shock and Dereangement in Blood Factors

Blood Loss Plasme

Shock Hemoglobin Hematocrit
Volume Protein
Grade % of normal % cells
% of Normal Gram%

I 14.4 3.9 20.0 5.2 42.5 1.7 6.6 0.1

II 20.7 4.3 29.7 4.1 38.4 1.5 6.4 0.1

III 34.3 3.5 46.1 3.4 34.6 1.0 6.2 0.1

IV 45.9 4.7 54.4 4.3 31.5 1.5 6.0 0.1

23
Factors Affecting :
PRELOAD
AFTERLOAD
CONTRACTILITY
HR/RHYTHM

Treatment
Limiting Infarct Size : dysrhytmias,
myocardial revascularization
Ballon angioplasty
Thrombolytic th/

24
 40% cases gram (-) bacteremia 40 90% mortality
endotoxin
Gram (+) exotoxin

CO , SVR Irreversible Hypotension

LVEF , RVEF
SV and LV Ejection Fraction
Mixed Venous O2 saturation N or
respiratory rate 25
 INFECTION SOURCE

PARENTERAL INVASION

RELEASE OF MEDIATORS OF SHOCK

1) DIRECT MYOCARDIAL EFFECTS 2) PERIPHERAL EFFECTS

a. LVEF
a. Vasodilatation
b. LV Dilatation
b. Vasoconstriction
c. Compliance Abnormalities
c. Leukocyte aggregation
d. Vascular endothelial dysfunction1

CARDIOVASCULAR EFFETS
a. Maldistribution of Blood Flow
b. Lactic Acid production
c. Mixed Venous O2

ULTIMATE OUTCOME PRODUCED Severe Multiple

Severe SVR Organ dysfx
Severe Myocardial Depression
26
D E AT H
 Monoclonal Antibodies
Naloxone
Prostaglandin Inhibitors
Lipid X
Antibodies to TNF
Protease inhibitors
Fluid + vasopressors
Inotropes, Epinephrine, dobutamine
Optimizing O2 transport correcting anemia

27
 O2 AIRWAY
BREATHING
CIRCULATION
OXYGEN TRANSPORT
Hb
CO DO2 CaO2 SaO2

OXYGEN EXTRACTION VO2

ScVO2
SmVO2 CmVO2

OXYGEN
CONSUMPTION
28
ENDOTRACHEAL
INTUBATION (SEDATIF)
AIRWAY PROTECTION
OXYGENATION
PATENCY
TOILET/SUCTIONING

29
 CONTROL VENTILATION,
SEDATION, RR
SaO2 > 93%
PaCO2 35 40 mmHg

30
 IV FLUID
RESUSCITATION
Crystalloid Isotonic/Colloid
POSITIONING
VASOPRESSOR/INOTROPIC
AGENT 31
 Management Shock
Hypovolemic
Recognize shock
Stop the bleeding !
Replenish intravascular volume
Restore organ perfusion

32
 Management Shock
Hypovolemic : Fluid Therapy
Warmed crystalloid/colloid solution
Rapid fluid bolus
- Adult : 2 liters Ringers lactate
- Child : 20 mL/kg Ringers lactate
Monitor response to initial therapy

33
 Management Shock
Hypovolemic : Vascular Access
2 large-caliber peripheral IVs
Central access
- Femoral
- Jugular
- Subclavian
Intraosseous
Obtain blood for crossmatch
34
 Minimal Arterial Sat.93-95%
Hb > 10 gram %
Inotropic and IV Fluid CO
SmVO2 and lactat Normal

35
 VITAL SIGN
CNS STATUS
SKIN PERFUSSION
URINARY OUTPUT
PULSE OXIMETRY

36